Relationship of antioxidant enzymes to ozone tolerance in branches of mature ponderosa pine (Pinus ponderosa) trees exposed to long-term, low concentration, ozone fumigation and acid precipitation

Seasonal activity of superoxide dismutase (SOD, EC 1.15.1.1). ascorbate peroxidase (APOD, EC 1.11.1.11) and guaiacol-oxidizing enzymes (GPODs, EC 1.11.1.7) was examined in needles of 12- to 15-year-old ponderosa pine (Pinus ponderosa Laws.) trees which received ozone (O₃) and acid precipitation treatment. Individual branches were enclosed in branch exposure chambers delivering either charcoal-filtered (O₃-reduced) air, ambient air, or air with twice ambient (2 x ambient) concentrations of O₃. Acid precipitation treatments were rain of pH 3.0 or 5.1 or no rain. Changes in antioxidant enzyme activity were not a consistent response to O₃ fumigation or acid precipitation, but when observed, they occurred most often in the O₃-sensitive clone and in symptomatic, fumigated branches. In the second year of fumigation. O₃ fleck symptoms appeared on needles of the sensitive clone as early as July and APOD activities were significantly increased by O₃ at all sampling dates. In the tolerant clone, antioxidant enzyme activities were not significantly changed by O₃ in the first season of fumigation (March to December 1990), not even during an episode when ambient O₃ concentrations reached 125 nl 1^?1 (240 nl 1^?1 in 2x ambient chambers). No foliar symptoms were observed on needles of the tolerant clone during this year. However, in the second year of fumigation (1992), O₃ fleck symptoms were observed on the tolerant clone and APOD activities were significantly increased in previous-year needles. The tolerant clone had SOD, APOD, and GPOD activities at least 40% higher than those of the sensitive clone before fumigation and 65, 178, and 119% higher, respectively, during both years of fumigation. The higher constitutive levels of these enzymes may have protected against foliar injury in 1990, however in 1992 we concluded that the stimulations in antioxidant enzyme activities observed in symptomatic branches of both clones were a consequence of O₃ injury. Total (intra- and extracellular) activities of the antioxidant enzymes did not appear to be good indicators of O₃ tolerance. Phenotypically, the O₃-tolerant clone was much more vigorous and in both years of fumigation, gas exchange rates were 30 to 71% higher than in the sensitive clone (P. D. Anderson, unpublished data). The greater vigor of the tolerant clone may allow more carbon allocation to protective and repair processes which include, but are not restricted to, the turnover of antioxidant enzymes and metabolites.